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VSV-FH is a **recombinant oncolytic virus** created by replacing the native glycoprotein (G) gene in vesicular stomatitis virus (VSV) with the genes encoding the fusion (F) and hemagglutinin (H) envelope proteins of measles virus[1][2][4]. This chimeric virus selectively targets and infects cancer cells overexpressing CD46, a cellular receptor commonly upregulated in various malignancies. VSV-FH exhibits improved tumor selectivity and robust oncolytic activity through induction of cell fusion (syncytia formation) and rapid replication, integrating anti-cancer mechanisms of both parental viruses: **rapid lytic apoptosis (VSV)** and **syncytia-mediated cell death (measles virus)**[1][2][3][4]. Preclinical studies demonstrate superior tumor cell killing, rapid propagation, and diminished neurotoxicity compared to parental VSV in hepatocellular carcinoma, myeloma, and other solid tumor models. Additional modifications have allowed further tumor targeting, such as retargeting the virus to specific tumor-associated receptors[4].
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